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Diphtheria is a rare but serious infectious disease. The bacteria usually causes infection of the throat and nose but can also cause skin infections. While some cases may be mild, the bacteria can produce dangerous toxins that cause severe complications which can be life-threatening. Such complications include heart trouble, paralysis, and kidney failure. Cases of diphtheria in New Zealand have declined significantly over the last century with very few cases reported in the last 50 years.

A brief history:

Diphtheria used to be common in New Zealand, with a total of 794 deaths in the five years from 1917 to 1921. Fortunately, in part because of vaccination, diphtheria has disappeared from New Zealand. However, it is common in other parts of the world and is, therefore, only a plane ride away.

The current New Zealand situation:

Since 1979, there have only been 4 confirmed diphtheria cases in New Zealand. These isolated cases occurred in 1987, 1998, 2002 and 2009.

It is believed that diphtheria vaccine protection wanes over time which is why the vaccine has been introduced into adult schedules in New Zealand. Diphtheria vaccine is included in the childhood immunisation schedule in New Zealand and remains an essential component of child vaccine programmes worldwide.

Symptoms:

Inflammation of the upper respiratory tract including the nose and throat. This may include sore throat, breathing problems, bloody or watery drainage from the nose, hoarseness, a bark-like cough, and painful swallowing.

Some cases will experience infection of the skin. This may include skin lesions.

However,some cases may not experience any symptoms.

How do you get it?:

Diphtheria is spread through close personal contact with someone who is infected or is a carrier of the bacteria who shows no symptoms. Spread commonly occurs through way of respiratory droplets (originating from a cough or a sneeze). The bacteria can also spread through contaminated objects or food.

What are the risks?:

The effects of diphtheria can range from mild to severe.
•For those infected, there is the potential for the diphtheria bacteria to release harmful toxins which can spread through the blood stream and affect major organs.
•Diphtheria toxin can cause significant damage to the heart, nerves, and kidneys.
•Diphtheria can be fatal. 5-10% of those infected die, even with treatment.

Who is most at risk?:

Those who are not immunised are at the greatest risk.

Crowded environments and poor hygiene are known to increase risk for diphtheria.

The majority of cases are reported in children under 10 years of age.

Treating the symptoms:

People suspected of having diphtheria will be given an antitoxin in a jab to the muscle or into the vein. Infection is then treated with antibiotics, such as erythromycin or benzathine penicillin. Additional treatment may include intravenous fluids, oxygen, bed rest, heart monitoring, use of a breathing tube, and correction of any blocked airways.

Preventing Disease Spread:

The person with diphtheria is excluded from school until they have recovered and had two negative throat swabs.

Contacts of the person with diphtheria are given antibiotics and may also need to have a booster vaccination with a diphtheria-toxoid containing vaccine

Contacts who are children are excluded from early childhood education, daycare, school and community activities until throat swabs shown they do not have the disease.

Adults who work with food or children are excluded from their work until throat swabs shown they do not have the disease.

Health Professionals

Causative organism:

Diphtheria is caused by the bacteria Corynebacterium diphtheriae. The toxin produced by some diphtheria bacteria can cause serious and life-threatening infections.

Clinical signs, symptoms and complications:

Membranous inflammation of the upper respiratory tract and nasopharynx, which may cause hoarseness, loss of voice or stridor (greyish membrane with a characteristic mousy smell). This may be accompanied by mildly painful tonsillitis or pharyngitis (90%).

Lymphadenopathy may lead to a “bull neck” appearance and the angle of the jaw may be obliterated. Unilateral or bilateral paralysis of the palatal muscles may lead to dysphagia

Skin and mucous membrane (mouth, vagina) lesions may occur in less serious disease. Pain, tenderness, and erythema at the site of infection progresses to ulceration with sharply defined borders and formation of a brownish grey membrane.

Infection by toxigenic strains may lead to toxin release, which can cause myocarditis, peripheral neuropathy with flaccid paralysis, renal failure secondary to tubular necrosis, stupor, coma and death.

Humans are the only known reservoir of diphtheria. The discharge from an infected person’s nose, throat, eye and skin lesions contains the bacteria and is contagious.

Transmission mostly happens from intimate contact with an infected person although fomites and food-borne sources can serve as vehicles of transmission.

Public health significance:

Diphtheria is rare in industrialised countries where immunisation programmes have run for decades. However, it's still common in some countries.

Since 1990, epidemic diphtheria has re-occurred through the Newly Independent States (NIS) of the former Soviet Union, including Russia, the Ukraine and the central Asian republics. In the 6 years from 1990 through 1995, the NIS accounted for more than 90% of all diphtheria cases reported to the World Health Organization from the entire world.

Illness is most common in low socio-economic groups living in crowded conditions. Infection can occur in immunised and partially immunised people, but disease is most severe in people who are not immunised.

An estimated 20% of those under 20 and 75% of those over 65 worldwide are thought to have insufficient immunity to diphtheria due to inadequate immunisation coverage and waning immunity.

While immunisation leads to the disappearance of toxigenic strains, non-toxigenic strains may become toxigenic through phage transmission. This makes the possibility of a resurgent diphtheria epidemic a real threat wherever there is insufficient community (herd) immunity.

New Zealand epidemiology:

Between 1917 and 1921 there were 794 reported deaths in non-Māori from diphtheria. Regular epidemics of infection occurred in New Zealand until 1950, and further outbreaks occurred in Milton and the Waikato in the 1960s.

In 1998 the first case of diphtheria was reported in New Zealand since 1979, and this was the first toxigenic isolate since 1987. In 2002 a four-year-old child was reported after a toxigenic strain was isolated from a hip aspirate. The child had no toxin related symptoms and had been fully vaccinated for age; this would not be regarded as a vaccine failure. In 2009 two cases of toxigenic diphtheria were isolted, the index case had acquired a tattoo in Samoa and the second case was a a household member ot the index case. There is no current data on the proportion of New Zealand adults susceptible to diphtheria.

The 1985 National Serum Survey found that 73 percent of five year olds, 65 percent of 10 year olds and 53 percent of 15 year olds had protective levels of diphtheria antibody. The decline apparent with age suggests that there is likely to be a large and increasing pool of adults susceptible to diphtheria in New Zealand. This was the reason for the introduction of adult tetanus diphtheria (Td) vaccination in 1994 and for the addition of adult tetanus/diphtheria boosters at 45 and 65 years in 2002.

Prevention:

People with diphtheria should be excluded from school until recovery and had two negative throat swabs.

Local health officials should be notified when cases of diphtheria occur. Public health measures include isolation of the contagious person and contact tracing to identify additional people who may be infected or at risk of infection.

Pharyngeal culture and prophylactic erythromycin or benzathine penicillin for close contacts.

Child contacts of the contagious person should be excluded from school, early childhood services and community gatherings until they are known to be culture negative.

Adult contacts who are food handlers or who work with children should be excluded from work until known to be culture negative.

Immunisation remains the only well-established mode of disease prevention. Diphtheria vaccination has been widely offered since World War II, leading to virtual disappearance of the disease in many countries.

Active immunisation against diphtheria is recommended during convalescence because having the disease does not necessarily convey immunity.

Fully immunised children aged up to and including six years, who are contacts of the contagious person, and who have only received three doses of diphtheria toxoid-containing vaccine within the last five years: give one injection of DTaP-IPV.

Fully immunised contacts aged seven years and older who have not received a booster dose of a diphtheria toxoid-containing vaccine within the last five years: if aged 7–15 years, give one injection of Tdap; if aged over 15 years, give one injection of Td or Tdap, the latter is not funded.

Treatment:

Diphtheria antitoxin is injected daily for 14 days for respiratory diphtheria. Sensitivity testing (skin or eye testing) should be conducted as only diphtheria antitoxin of equine origin is available.

Benzathine penicillin or erythromycin is used to eliminate the bacteria, reduce toxin production and decrease infectivity. Intravenous antibiotics are used until the person is able to swallow oral antibiotics comfortably. The use of antibiotics is in addition to daily antitoxin injections.

Additional treatment may include intravenous fluids, oxygen, bed rest, heart monitoring, use of a breathing tube, and correction of any blocked airways.

Disease Effects vs Vaccine Side Effects (Table)

Disease Description:

Diphtheria is a rare but serious bacterial illness that usually causes infection of the throat and nose but can also cause skin infections.

Redness and/or swelling more than 6 cm in size around the injection site.
In a small percentage of vaccine recipients the reactions will be severe enough to limit movement of the arm and may last for about a week.

Swelling involving the entire thigh or upper arm occurs in 2–3 percent of children after administration of the fourth and fifth doses of acellular pertussis vaccine. It resolves spontaneously without long term consequences.

ADT™ Booster is used for primary and booster vaccination of children 7 years of age and over and adults to protect against tetanus and diphtheria. An alternative vaccine called Boostrix®, which protects against tetanus, diphtheria and pertussis (whooping cough), can be substituted for one, two or all three doses of the primary vaccinations in these age groups. Both ADT™ Booster and Boostrix® are licensed as booster vaccines. They are used for primary vaccination out of licensure as there is no alternative primary vaccination strength vaccine available in New Zealand for these age groups. When the vaccine is used for a primary vaccination course, use will be outside of current licensure. No safety concerns are expected with use in these circumstances.

Infanrix®-IPV is used for primary and booster vaccination of infants and children to protect against diphtheria, tetanus, pertussis and poliomyelitis. Infanrix®-IPV can also be used for catch-up immunisation for children up to their 10th birthday.

Boostrix® is used for booster vaccination of adolescents aged 11 years and pregnant women between 28-38 weeks gestation* to protect against diphtheria, tetanus and pertussis (whooping cough). Boostrix® can also be used for catch-up immunisation for children aged 7 years# to under 18 years.

*After immunisation protection against pertussis takes up to two weeks to develop. Whilst immunisation between 38-40 weeks gestation is still safe for mother and baby later immunisation means the newborn may still be exposed to the disease by their mother on delivery and/or during the first two weeks of life. The PHARMAC decision to limit funded Boostrix® to 28-38 weeks gestation maximises the benefit of immunisation against pertussis whilst being accountable for the use of public funds. Pregnant women can choose to purchase Boostrix® privately after 38 weeks gestation or at any time after delivery.

#Although Boostrix® is not licensed for use in children aged 7 years to under 10 years it has been used in New Zealand and overseas in this age group and there are no safety concerns with off-label use.

Tetanus, also called lockjaw, is caused by the action of tetanus toxin released by a spore-forming bacillus called Clostridium tetani. The bacillus and spores are found the soil around the world. Many animals, in addition to humans, can carry the bacillus and its spores in their gastrointestinal tract and excrete them in faeces. Tetanus occurs after the bacillus and/or spores are introduced into the body through a wound and release a toxin that affects the nervous system.

A person or animal with tetanus is not infectious. Having tetanus does not usually generate immunity to the disease.

A brief history:

The first medical description of tetanus is believed to have been recorded in ancient Egypt. Later tetanus was also described by Hippocrates and other ancient Greeks but the cause was not discovered until 1884. Worldwide at least one million cases of tetanus need hospital treatment each year. In developing countries neonatal tetanus (acquired through the umbilical stump) accounts for approximately half the cases. In developed countries injuries cause approximately 70% of cases.
On a weight basis tetanus toxin is one of the most potent known poisons.
Universal infant immunisation with a tetanus toxoid vaccine began in 1960 in New Zealand. Anyone born before 1960 is less likely to have received a primary series, unless they were in the armed forces.

The current New Zealand situation:

Almost all the recent cases of tetanus in New Zealand, in both adults and children, occurred in individuals without a documented history of a primary immunisation course of a tetanus-containing vaccine.

Seven cases of tetanus were notified in 2010, the highest number since 1992, and one person died. One case had received a primary course of tetanus vaccines but had not had a booster dose for 15 years. In New Zealand tetanus usually occurs following a minor injury.

Symptoms:

Initial symptoms include weakness, stiffness or cramps and difficulty chewing or swallowing food. As the disease progresses tetanus is characterised by muscular rigidity and very painful contraction spasms. When severe it is associated with a characteristic facial grimace (risus sardonicus) and arching of the back (opisthotonus).

How do you get it?:

Animals, including humans, can carry Clostridium tetani in their intestine and excrete the bacillus and/or spores with their faeces into the soil. The bacillus and/or spores can be introduced into the body through any break in the skin (wound), no matter how minor.

Once in the wound bacilli mature, become spores and germinate releasing a chemical that is toxic to the central and autonomic nervous systems (toxin).

Wounds that are contaminated, have lots of tissue damage or a deep puncture type wounds have the highest risk of containing Clostridium tetani but even minor wounds have caused tetanus.

What are the risks?:

Approximately 10% of people who get tetanus die, despite the modern intensive care units, machines and medicines.

Those who survive usually have a full recovery after physical rehabilitation.

Who is most at risk?:

Everyone who has not received a primary course of three tetanus containing vaccines.

Anyone born before 1960 is less likely to have received a primary series, unless they were in the armed forces. Older women appear to be at particular risk.

It is not possible to eliminate Clostridium tetani from the environment. All wounds require adequate cleaning and removal of damaged tissue. Additional treatment depends on the circumstances of each case.

A complete primary course of three doses of tetanus containing vaccine and appropriate administration of booster doses provides protection against the toxin released by the spores but will not stop infection with the bacillus and/or spores, their germination or toxin release.

Tetanus immunoglobulin (TIG), derived from human blood donations, must be given to any person who has not completed three doses of vaccine before getting a high tetanus risk wound. The person should also start a course of tetanus containing vaccines or continue their course of tetanus containing vaccines until they have had three doses.

A person who has completed three doses of tetanus containing vaccine before having a high tetanus risk wound may benefit from a booster with a tetanus containing vaccine if they have not had a tetanus containing vaccine in the previous five years.

A person who has completed three doses of tetanus containing vaccine before having a low tetanus risk wound may benefit from a booster with a tetanus containing vaccine if they have not had a tetanus containing vaccine in the previous 10 years.

People in certain occupations and travellers may also benefit from tetanus vaccine booster doses when more than 10 years have elapsed since their previous dose.

Tetanus is caused by toxin released from Clostridium tetani, a gram-positive, spore-forming, anaerobic bacillus. Animals, including humans, can carry Clostridium tetani bacillus and spores in their intestine and excrete them in faeces. Spores are found in soil worldwide and can survive for months to years if not exposed to sunlight. They are resistant to boiling and a variety of disinfecting agents. Sterilisation of equipment at 120°C for 15 to 20 minutes more easily destroys the spores.

Clostridium tetani need an anaerobic (absent oxygen) environment in which to grow, often found in damaged and necrotic tissue, and prefer a growing temperature of 33-37°C. The bacillus becomes a spore that germinates and releases two exotoxins, tetanolysin and tetanospasmin. Of these tetanospasmin is the neurotoxin that causes the symptoms of tetanus. On a weight basis tetanospasmin is one of the most potent known poisons.

Clinical signs, symptoms and complications:

Incubation of Clostridium tetani ranges from 3-21 days, with the average being around 8-10 days. The distance between the point of bacillus entry (wound) and the central nervous system (CNS) influences the incubation period, with the further the wound is from the CNS the longer the incubation period.

Wounds of the head, neck and trunk typically have the shortest incubation periods. The length of incubation period also influences the severity of the disease, longer incubation (10 days or more) typically results in more mild disease than a shorter incubation period (7 days or less).

Tetanus is diagnosed on clinical grounds. A history of contaminated wound may or may not be present. Laboratory testing e.g., wound cultures, cannot confirm or exclude the diagnosis. Strychnine poisoning mimics tetanus, without a raised body temperature. Other differential diagnoses include dental caries/disease, tonsillitis, parotitis, temporomandibular joint (TMJ) disease, Bell’s palsy, low serum calcium and dystonic reactions to medication.

Tetanospasmin travels to the CNS via the axons and irreversibly binds to the neuromuscular junction nerve terminals, blocking the release of inhibitory neurotransmitters that cause muscle relaxation. Tetanospasmin may also cause autonomic nervous system (ANS) dysfunction.
Localised tetanus is rare in humans; spasms are confined to an area close to the wound, may be mild and may resolve spontaneously over several weeks to months or may progress to generalised tetanus.

Generalised tetanus is characterised by generalised muscular rigidity and prolonged, tonic contraction spasms often triggered by external stimuli. Initial symptoms include weakness, stiffness or cramps, and difficulty chewing or swallowing food progressing to the person’s inability to open their mouth (trismus), a characteristic facial grimace (risus sardonicus) and arching of the back (opisthotonus).

The person with tetanus may cause trauma to their tongue. Muscle spasms can be severe enough to cause fractures of the vertebrae and long bones and can raise the person’s body temperature by 2-4°C.

A person with tetanus remains conscious and alert, unless they develop upper airway obstruction and become severely hypoxic. Spasm of the glottis can cause immediate death.

Cephalic tetanus is rare and usually associated with a wound on the head. Following a short incubation period, 1-2 days, the person presents with atonic cranial nerve palsies (facial paralysis) involving nerves III, IV, VII, IX, X and XII, singly or in combination. Trismus may be present and cephalic tetanus may progress to generalised tetanus.

Tetanus neonatorum (neonatal tetanus) is the most common presentation of tetanus in developing countries. It is a form of generalised tetanus arising from infection of the umbilical stump. Mortality exceeds 90%. Babies who survive may experience long term consequences including subtle intellectual and behavioural abnormalities, cerebral palsy and severe psychomotor retardation.

The acute clinical course of tetanus varies between 1-4 weeks. Approximately 10% of people who get tetanus die, despite the modern intensive care units, machines and medicines. Those who survive usually have a full recovery after rehabilitation.

Method of transmission:

Animals, including humans, can carry Clostridium tetani in their intestine and excrete the bacillus and/or spores with their faeces into the soil. The bacillus and/or spores can be introduced into the body through any break in the skin (wound), no matter how minor. Once in the wound bacilli mature, become spores and germinate releasing toxic to the central nervous system (toxin).

A person with tetanus is not infectious to others.

Public health significance:

It is not possible to eliminate Clostridium tetani from the environment.

A complete primary course of three doses of tetanus containing vaccine and appropriate administration of booster doses provides protection against the toxin released by the spores but will not stop infection with the bacillus and/or spores, their germination or toxin release.

Vaccination against tetanus provides individual protection against tetanus.
Vaccination against tetanus does not create “herd immunity” because the disease is not spread person to person.

All cases of tetanus must be notified immediately on suspicion to the local medical officer of health, who should be provided with as accurate immunisation history as possible.

New Zealand epidemiology:

Almost all the recent cases of tetanus in New Zealand, in both adults and children, occurred in individuals without a documented history of a primary immunisation course of a tetanus-containing vaccine.

Seven cases of tetanus were notified in 2010, the highest number since 1992. One case aged 1-4 years (unvaccinated); one case 40-49 years (last vaccination 15 years earlier); one case aged 60-69 years (vaccination status unknown; and four cases aged 70 years and older (two unvaccinated, two vaccination status unknown). One of the people aged over 70 years died from tetanus.

The National Serosurvey of Vaccine Preventable Diseases over 2005-2007 found that 85 percent of 6–10-year-olds, 94 percent of 11–15-year-olds, 95 percent of 16–24-year-olds, 95 percent of 25–44-year-olds and 89 percent of ≥ 45-year-olds had presumed protective levels of tetanus antibody.

Prevention:

Wounds that are contaminated (dirt, faeces, saliva, foreign bodies e.g., wood splinter), have lots of tissue damage (crush injuries, burns), are a deep puncture type wound and/or are more than six hours old have the highest risk of containing Clostridium tetani and causing tetanus, but even minor wounds have caused tetanus.

All wounds require adequate cleaning and removal of damaged tissue. Additional treatment depends on the circumstances of each case.

Management of high tetanus risk wounds

If a wound is considered to be a high tetanus risk wound and the person has not previously completed a three dose course of tetanus containing vaccine or there is any doubt with regard to the person having already completed a three dose course of tetanus containing vaccine tetanus immunoglobulin (TIG) must be given.

Outside of Auckland, TIG is ordered from the local District Health Board hospital blood bank. Within Auckland TIG is ordered directly from the New Zealand Blood Service.

If less than 24 hours has elapsed since the wound occurred the recommended dose of TIG, to prevent tetanus, is 250 IU administered by intramuscular injection. However, the dose should be increased to 500 IU in cases of severely contaminated wounds, burns and/or when more than 24 hours has elapsed since the wound occurred.

Antibiotics are not currently recommended for prevention of tetanus. However wounds should be observed regularly for signs of infection and antibiotics prescribed when clinically indicated.

People with tetanus do not need to be isolated.

Contacts of a person with tetanus do not need a tetanus booster.

A person who has completed three doses of tetanus containing vaccine before having a high tetanus risk wound may benefit from a booster with a tetanus containing vaccine if they have not had a tetanus containing vaccine in the previous five years.

Management of low tetanus risk wounds

A person who has completed three doses of tetanus containing vaccine before having a low tetanus risk wound may benefit from a booster with a tetanus containing vaccine if they have not had a tetanus containing vaccine in the previous10 years.

Occupational vaccination and travel

People in certain occupations and travellers may benefit from tetanus vaccine booster doses when more than 10 years have elapsed since their previous dose.

Prevent circulating toxin affecting the CNS and ANS
Tetanus immunoglobulin (TIG) or normal human immunoglobulin (IVIG) is given at diagnosis of the disease.
Patients should commence, or complete, a course of three tetanus containing vaccinations because the amount of tetanospasmin able to cause disease is very small and not expected to induce immunity. The Clostridium tetani spores are very stable, retaining their ability to germinate and cause disease in the future. Cases of tetanus relapse or recurrence have been reported.

C​ontrol muscle spasms
Keeping the patient in a dimly lit and quiet environment to avoid sudden stimulus. Medication to reduce spasms and hypertonicity if clinically indicated and pain management e.g., use of beta-blockers and morphine.

Manage respiratory function
Patients with severe spasms that affect breathing may need neuromuscular blockade and mechanical ventilation. A tracheostomy may be required if long term ventilation is anticipated.

Tetanus spores in a wound germinate and release toxin that affects the nervous system.

Effects of disease:

Initial symptoms include weakness, stiffness or cramps and difficulty chewing or swallowing food.

Symptoms progress to muscle rigidity and very painful contraction spasms with an inability to open the mouth (trismus), a characteristic facial grimace (risus sardonicus) and arching of the back (opisthotonus).

Trauma to the tongue during spasms.

Bone fractures.

Raised body temperature by 2-4°C.

Blood pressure changes.

Heart rate and rhythm changes.

Sweating.

Unable to pass urine.

Throat spasm.

Approximately 10% of people who get tetanus die.

Those who survive usually have a full recovery after rehabilitation.

Common side effects of vaccine:

Soreness/pain, redness and/or swelling around the injection site.

Fever over 38°C.

Decreased appetite, vomiting and/or diarrhoea.

Irritability, restlessness.

Unusual crying.

Fatigue.

Redness and/or swelling more than 6 cm in size around the injection site.
In a small percentage of vaccine recipients the reactions will be severe enough to limit movement of the arm and may last for about a week.

Swelling involving the entire thigh or upper arm occurs in 2–3 percent of children after administration of the fourth and fifth doses of acellular pertussis vaccine. It resolves spontaneously without long term consequences.

Pertussis, commonly known as whooping cough, is a highly infectious bacterial infection spread by coughing and sneezing. It causes severe bouts of coughing, which may be accompanied by vomiting and a whooping sound. Pertussis can last up to 3 months and is sometimes referred to as the ‘100 day cough.’ The symptoms are more obvious in children, because infants and adults are less likely to ‘whoop.’

The current New Zealand situation:

New Zealand has epidemics every 3-5 years with several thousand cases (mostly young children) reported in each epidemic. Older adolescents and adult pertussis often goes unrecognised and is often under reported. Up to a third of adolescents and young adults with a persistent cough have evidence of recent pertussis infection.

Symptoms:

Pertussis can be divided into three stages:

The initial stage, following the incubation stage, is called the catarrhal stage is the most infectious. It lasts 7-10 days and can include a runny nose, sneezing, slight fever, and a mild irritating cough.

The second stage or paroxysmal stage usually lasts 2-4 weeks, but can persist for up to 10 weeks. A paroxysm is a spasm of coughing followed by a big breath in or high pitched whoop in children. Infants and adults generally do not have the characteristic 'whoop' sound. Infants and young children often appear very ill, and may turn blue and vomit with coughing bouts.

The convalescent stage may last for months. Although the cough eventually disappears after several weeks, coughing fits may recur whenever the patient suffers any subsequent respiratory infection.

How do you get it?:

Pertussis is highly contagious and is spread by coughing and sneezing. It infects around 90% of non-immune household contacts and 50 to 80% of non-immune school contacts. Many babies catch it from their older siblings or parents - often before they are old enough to be fully vaccinated.

What are the risks?:

Around five in 10 babies who catch pertussis before the age of 12 months require hospitalisation and 1-2 in 100 of those hospitalised die from pertussis infection. Severe coughing can temporarily stop the oxygen supply to the brain (hypoxia). In around two in 1000 children pertussis leads to permanent brain damage, paralysis, deafness or blindness. Secondary infections such as pneumonia and ear infections can occur.

The disease is usually milder in adolescents and adults, consisting of a persistent cough similar to that found in other upper respiratory infections, although some adults will collapse or experience a rib fracture from violent coughing. Both hospitalisations and deaths are likely to be under-estimated in adults due to the lack of the ‘whooping’ sound.

Who is most at risk?:

Those most at risk of serious disease are infants under 12 months of age. Infants who do not receive doses of pertussis containing vaccine at the scheduled times of 6 weeks, 3 months, and 5 months have up to a five-fold increased risk of being hospitalised with pertussis.

Preventing Disease Spread:

On-time immunisations for infants at 6 weeks, 3 months and 5 months in addition to children receiving boosters at four years and 11 years is the best prevention.

If a pregnant woman has high levels of circulating protection against whooping cough during the last weeks of pregnancy some of this will pass through the placenta and may protect the newborn from severe whooping cough for up to six weeks after delivery. A tetanus, diphtheria, whhoping cough booster immunisation (Boostrix®) is recommended and free for women between 28-38 weeks of pregnancy through their Doctor.

Breastfeeding does not provide direct protection against whooping cough.

Antibiotics do not cure pertussis but are given to reduce the spread of infection to others.

All cases of pertussis should be excluded from early childhood services, school, or community gatherings until they are well enough to attend and have either received five days of antibiotics or three weeks have elapsed since the onset of coughing spasms.

Pertussis is caused by a bacterium, Bordetella pertussis; a gram-negative bacillus, which colonises the upper respiratory tract. There are other organisms such as Bordetella parapertussis, Mycoplasma pneumoniae and Chlamydia pneumoniae, which can cause a pertussis-like illness.

Clinical signs, symptoms and complications:

Pertussis disease can be divided into three stages:

Catarrhal stage

Can last 7-10 days and includes a runny nose, sneezing, low-grade fever, and a mild cough (all similar symptoms to the common cold).

Paroxysmal stage

Usually lasts 1-6 weeks, but can persist for up to 10 weeks.

The characteristic symptom is a burst, or paroxysm, of numerous, rapid coughs.

At the end of the paroxysm the patient suffers from a long inhaling effort that is characterized by a high-pitched whoop.

Infants and young children often appear very ill and distressed, and may turn blue and vomit. Infants generally do not have the characteristic “whoop” sound.

Convalescent stage

May last for months.

Although the cough usually disappears after 2-3 weeks, paroxysms may recur whenever the patient suffers any subsequent respiratory infection.

Disease is more severe in infants and young children.

The cough may persist for up to 3 months and is often associated with vomiting.

Severe coughing may lead to brain hypoxia. In 1-3 per 1000 children, whooping cough leads to permanent brain damage, paralysis, deafness or blindness.

The disease is usually milder in adolescents and adults, consisting of a persistent cough similar to that found in other upper respiratory infections. However, these individuals are still able to transmit the disease to others, including unimmunised or incompletely immunised infants.

Pertussis immunity wanes over time; both following natural disease and vaccination (immunity lasts 4–10 years). Re-infection may present as a persistent cough, rather than typical pertussis.

Method of transmission:

Pertussis is spread through the air by infectious droplets and is highly contagious infecting 90% of susceptible household contacts and 50 to 80% of susceptible school contacts. The incubation period is commonly 7-10 days, with an upper limit of 21 days. Many babies contract pertussis from their older siblings or parents.

Public health significance:

Pertussis kills about 250,000 children worldwide each year. Many children are left with brain damage from pertussis infection. Pertussis is highly infectious and around 90% of non-immune household contacts will contract it.

Most countries have epidemics every three to five years.

Both hospitalisation and deaths from pertussis are likely to be underestimated as infants, particularly preterm, may either present without characteristic symptoms or be misclassified as sudden infant death syndrome.

It has been estimated that up to 20% of severe adult coughs 1-3 months untreated, could be caused by pertussis infection. These individuals are a significant reservoir of infection.

Some countries such as USA, Australia and Canada are now identifying higher rates of pertussis infection, especially in adolescents and adults. The cause of this is not yet fully explained however these countries are introducing pertussis boosters for adolescents.

Those most at risk are young babies. Around 50% of those who catch pertussis before the age of 12 months require hospitalisation. Children under 12 months who are ill enough to be admitted to hospital have a 1-2 in 100 chance of dying.

Currently available vaccines prevent disease much better than they prevent infection. They will not eradicate pertussis but in countries with very high immunisation coverage rates (>95%), the three to fiuve yearly epidemics affect fewer individuals and the resultant disease is less severe than in unvaccinated communities.

New Zealand epidemiology:

The estimated pertussis case fatality rate in New Zealand for the period 1970 to 1992 was 0.4 percent. This is comparable to reported case fatality rates from the UK and the US over a similar period. There were no deaths from pertussis in New Zealand between 1988 and 1995, one death in 1996, and since 1999 there has been one death each year up to 2004. Morbidity from pertussis in New Zealand has been described primarily using hospital discharge data. National passive surveillance data has been available since 1996, when pertussis became a notifiable disease. Comparison of notification and hospitalisation data from 1996 and 1997 demonstrates that fewer than 50 percent of hospitalised cases are notified. The three to four year periodicity of pertussis epidemics in New Zealand is similar to that seen in many other countries. The decrease in the pertussis hospitalisation rate that occurred following the introduction of mass immunisation has not been sustained.

Prevention:

There is almost no maternal protection passed to the newborn against pertussis via breastmilk.

Cases should be excluded from school or daycare until the infectious period is over (21 days from the onset of coughing or after 5 days of antibiotics). Some countries recommend health care workers and/or daycare workers with confirmed pertussis infection be placed on sick leave until fully recovered.

Pertussis vaccines were initially developed in the 1940s.

There are two types of pertussis vaccine commonly used internationally: whole cell pertussis vaccine (wP) and acellular vaccine (aP). Both vaccines have similar efficacy but acellular vaccines cause significantly fewer adverse reactions than whole cell vaccines. Where feasible and available, acellular vaccines should be used in preference to whole cell vaccines.

Acellular pertussis-containing vaccines have now replaced whole-cell vaccines in many countries, including New Zealand. There are a number of acellular pertussis vaccines, which contain three or more purified components of B. pertussis: pertussis toxin (PT), filamentous haemagglutinin (FHA), pertactin (PRN), and fimbrial antigens or agglutinogens.

Treatment:

Antibiotics have no role in treating pertussis. However they are given to reduce transmission of the organism and may be given to all household and other close contacts of the patient.

Identification of pertussis infection and prescription of antibiotics for women in the third trimester of pregnancy minimises the spread to non-immune infants in the first month of life.

Disease Effects vs Vaccine Side Effects (Table)

Disease Description:

Pertussis is a highly infectious bacterial disease of the respiratory system. Symptoms inlcude a severe cough which can last for many weeks. Pertussis is very serious in young infants.

Effects of disease:

Secondary infections such as pneumonia and ear infections can occur.

Around 5 in 10 infants who catch pertussis before the age of six months require hospitalisation.

Severe coughing can temporarily stop the oxygen supply to the brain (hypoxia).

Around 1-2 in 100 hospitalised infants younger than 12 months die.

Around 2 in 1000 children with paroxysmal cough develop permanent brain damage, paralysis, deafness or blindness.

Urinary incontinence in adults

Some adults will collapse or experience a rib fracture from violent coughing.

Common side effects of vaccine:

Soreness/pain, redness and/or swelling around the injection site.

Fever over 38°C.

Decreased appetite, vomiting and/or diarrhoea.

Irritability, restlessness.

Unusual crying.

Fatigue.

Redness and/or swelling more than 6 cm in size around the injection site. In a small percentage of vaccine recipients the reactions will be severe enough to limit movement of the arm and may last for about a week.

Swelling involving the entire thigh or upper arm occurs in 2–3 percent of children after administration of the fourth and fifth doses of acellular pertussis vaccine. It resolves spontaneously without long term consequences.